Chronic obstructive pulmonary disease (COPD) is a lung disease that causes narrowing of the airways due to an abnormal inflammatory response in the lung. It is known that chronic obstructive pulmonary disease is caused mainly by inhalation of noxious particles or gases, and particularly, smoking is the major cause of chronic obstructive pulmonary disease. Currently, the prevalence of chronic obstructive pulmonary disease among people aged over 40 years in Korea is increasing every year. In addition, chronic obstructive pulmonary disease is the only disease with increasing incidence and prevalence worldwide, and is anticipated to become the third leading cause of death in 2020 worldwide. Smoking acts as a potent stimulus in lung tissue to increase the production of various proinflammatory factors, growth factors, oxidants and chemotactic factors and activate inflammatory signaling systems to thereby stimulate the migration of numerous inflammatory cells, including neutrophils and macrophages, thereby making lung inflammation worse. Proteases such as metalloproteinase derived from cigarette smoke and inflammatory cells are activated to destroy structures in interstitial tissue. This results in abnormal changes in lung tissue, for example, airway wall thickening and pulmonary fibrosis, which deteriorate lung function. Thus, various agents for the prevention and treatment of chronic obstructive pulmonary disease have been developed with a focus on alleviation of lung inflammation that is the major cause of the disease. Among them, treatment with steroidal agents and antibiotics for alleviation of inflammation in chronic obstructive pulmonary disease can be a very attractive treatment method, similar to asthma treatment. However, steroidal agents and antibiotics have limitations in that they can cause many side effects due to immune suppression and tolerance, and thus are not suitable for chronic obstructive pulmonary disease patients in need of long-term treatment.
EC-18, as a kind of monoacetyldiglyceride compounds, was separated or extracted from the natural deer antler. EC-18 is known to be hematopoiesis. Also, it is known that EC-18 increases survivability ratio of animals in sepsis animal model experiment using cecal-ligation-puncture, and shows no-toxicity in GLP (Good Laboratory Practice) toxicity test. However, the effect of monoacetyldiacylglycerol compounds including EC-18 is not known or disclosed in chronic obstructive pulmonary disease. Accordingly, the present inventors have made extensive efforts to develop an agent for treating chronic obstructive pulmonary disease, which is derived from a natural material or is a new compound. As a result, the present inventors have found that a monoacetyldiacylglycerol compound inhibits secretion of CXCL-1, TNF-α or MIP-2 and inhibits infiltration of inflammatory cells into bronchi, and thus can be effectively used for the prevention or treatment of chronic obstructive pulmonary disease, thereby completing the present invention.